Endocrinology of sex steroid hormones and cell dynamics in the periodontium

Mariotti, Angelo; Mawhinney, Michael G.

doi:10.1111/j.1600-0757.2011.00424.x

Cited by 79 publications

(91 citation statements)

References 186 publications

(266 reference statements)

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“…A growing body of evidence suggests that androgens and estrogens modulate periodontal tissues, but the specific relationship between sex hormones and periodontal endocrinopathies remains to be determined . Some mechanisms have been proposed to explain the regulation of periodontal disease by those hormones: (i) sex steroid hormones would increase a periodontopathogenic microbiota; (ii) sex steroid hormones would promote an alteration in vascular characteristics; (iii) periodontal tissues responses would be exacerbated by immune‐endocrine interactions; (iv) specific populations of fibroblasts and epithelial cells would be modulated by sex steroid hormones . However, the host response in a multifactorial disease, such as the periodontal disease, most probably cannot be simplified and represented by one mechanism of action only, but rather by a combination of them.…”

Section: Discussionmentioning

confidence: 99%

“…Androgenic hormones include androstenedione, androstenediol, TES and DHT. One of the most important androgens is TES, which is synthesized by the Leydig cells (in men), tecal cells in the ovaries (in women) and the adrenal cortex . Testosterone acts directly via binding to androgen receptors, or indirectly being converted into DHT or estradiol.…”

Section: Discussionmentioning

confidence: 99%

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The role of androgens on periodontal repair in female rats

Steffens

Santana

Pitombo

et al. 2018

Journal of Periodontology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The role of androgens on periodontal repair in female rats

Steffens

Santana

Pitombo

et al. 2018

Journal of Periodontology

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“…Puberty has a transient effect on the inflammatory status of the gingiva, but the severity or the time of onset of gingival inflammation varies in different studies [30]. Severity of gingivitis during the pregnancy can be increased independently from dental plaque accumulation [31].…”

Section: Discussionmentioning

confidence: 99%

Association between Polycystic Ovary Syndrome, Oral Microbiota and Systemic Antibody Responses

et al. 2014

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Polycystic ovary syndrome (PCOS) is a hormonal disorder of women that not only is the leading cause of infertility but also shows a reciprocal link with oral health. This study aimed to investigate the hypothesis that the levels of putative periodontal pathogens in saliva and their antibody response in serum are elevated in PCOS, compared to systemic health. A total of 125 women were included in four groups; 45 women with PCOS and healthy periodontium, 35 women with PCOS and gingivitis, 25 systemically and periodontally healthy women, 20 systemically healthy women with gingivitis. Salivary levels of seven putative periodontal pathogens were analyzed by quantitative real-time polymerase chain reaction and serum antibody levels were analyzed by ELISA. In women with PCOS, salivary Porphyromonas gingivalis, Fusobacterium nucleatum, Streptococcus oralis and Tannerella forsythia levels were higher than matched systemically healthy women, particularly in the case of gingivitis. Aggregatibacter actinomycetemcomitans and Treponema denticola levels were similar among study groups. The presence of PCOS also enhanced P. gingivalis, Prevotella intermedia and S. oralis serum antibody levels, when gingivitis was also present. Gingival inflammation correlated positively with levels of the studied taxa in saliva, particularly in PCOS. The presence of P. gingivalis and F. nucleatum in saliva also exhibited a strong positive correlation with the corresponding serum antibody levels. In conclusion, as an underlying systemic endocrine condition, PCOS may quantitatively affect the composition of oral microbiota and the raised systemic response to selective members of this microbial community, exerting a confounding role in resultant gingival inflammation and periodontal health. The most consistent effect appeared to be exerted on P. gingivalis.

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“…Puberty and the menopause are associated with a higher prevalence of periodontal diseases in females (certainty low) (Armitage 2013, Mariotti & Mawhinney 2013.…”

Section: Hormonal Changes In Femalesmentioning

confidence: 99%

Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases

Chapple

Bouchard

Cagetti

et al. 2017

J Clinic Periodontology

388

369

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Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self‐esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio‐economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management. Aim To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases. Methods One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report. Results & Conclusions There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor (VDR), Fc gamma receptor IIA (Fc‐γRIIA) and Interleukin 10 (IL10) genes. For caries, genes involved in enamel formation (AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics (AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end‐products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub‐optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases.

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Endocrinology of sex steroid hormones and cell dynamics in the periodontium

Cited by 79 publications

References 186 publications

The role of androgens on periodontal repair in female rats

The role of androgens on periodontal repair in female rats

Association between Polycystic Ovary Syndrome, Oral Microbiota and Systemic Antibody Responses

Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases

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